Anti-CD30 monoclonal antibody linked via a cleavable valine-citrulline linker to monomethyl auristatin E (MMAE). After binding CD30 and internalization by CD30-positive cells, the linker is proteolytically cleaved to release MMAE, which binds tubulin, blocks microtubule polymerization, causes G2/M arrest, and induces apoptosis.
NO
INDIRECT
The ADC targets CD30, is internalized, and releases MMAE, which binds the Vinca site on beta-tubulin to block microtubule polymerization and cause G2/M arrest and apoptosis. Beta-tubulin expression alone is not sufficient; CD30-mediated delivery is required.
Autologous, genetically modified CAR T-cell therapy targeting GPRC5D. Patient T cells are engineered to express an anti-GPRC5D chimeric antigen receptor with CD3ζ and co-stimulatory signaling domains; CAR engagement activates T cells, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPRC5D-expressing malignant plasma cells.
Autologous T cells are genetically engineered to express an anti-GPRC5D chimeric antigen receptor with CD3ζ and co-stimulatory domains. Upon binding GPRC5D on malignant plasma cells, the CAR activates T-cell signaling, leading to expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells.
YES
DIRECT
CAR T cells bind GPRC5D on target cells, form an immunologic synapse, and kill via perforin/granzyme-mediated apoptosis (with T-cell activation and cytokine release).
Autologous peripheral blood lymphocytes genetically engineered to express T-cell receptors specific for KRAS G12D or G12V neoantigens (HLA class I/II–restricted) to recognize mutant KRAS peptides and kill tumor cells.
Autologous T cells are genetically engineered to express HLA class I/II-restricted T-cell receptors specific for KRAS G12D or G12V neoantigen peptides; binding of these mutant KRAS peptides on tumor cells triggers T-cell activation and cytotoxic killing (perforin/granzyme-mediated lysis) of the target cells.
YES
DIRECT
Engineered TCR T cells recognize the HLA-presented KRAS G12D peptide and directly kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous peripheral blood lymphocytes genetically engineered to express T-cell receptors specific for KRAS G12D or G12V neoantigens (HLA class I/II–restricted) to recognize mutant KRAS peptides and kill tumor cells.
Autologous T cells are genetically engineered to express HLA class I/II-restricted T-cell receptors specific for KRAS G12D or G12V neoantigen peptides; binding of these mutant KRAS peptides on tumor cells triggers T-cell activation and cytotoxic killing (perforin/granzyme-mediated lysis) of the target cells.
YES
DIRECT
Engineered TCR-transduced T cells recognize the HLA-presented KRAS G12V peptide on tumor cells and kill them via perforin/granzyme-mediated cytotoxicity (apoptosis/lysis).
KRAS-targeted adenoviral vector vaccine used as a prime to induce and expand KRAS-mutant–specific T cells.
A non-replicating adenoviral vector delivers genes encoding shared KRAS-mutant neoantigens to antigen-presenting cells, leading to intracellular expression and MHC I/II presentation of the neoantigen peptides. This primes and expands KRAS-mutant–specific CD8+ and CD4+ T cells, promoting cytotoxic T‑cell responses against KRAS‑mutant tumor cells (used as a prime prior to an mRNA boost).
YES
INDIRECT
Vaccination primes/expands endogenous KRAS G12D–specific CD8+ T cells, which recognize KRAS G12D peptide presented on MHC and kill target-expressing tumor cells via perforin/granzyme (and Fas–FasL) cytotoxicity.